NEONATAL SEIZURES

 

Definition of Neonatal Seizures

  • A stereotypic, paroxysmal spell of altered neurologic function

(behavior, motor, and/or autonomic  function)

  • Neonatal period limited to :

– first 28 days for term infants

– 44 weeks gestational age for pre-term

First sign of neurological dysfunction

Powerful predictors of long-term cognitive and developmental impairment

Frequency

  • Incidence of seizures higher in the neonatal period than in any other age group

 Why do neonatal seizures have such unusual presentations?

 

  • Immature CNS cannot sustain a synchronized, well orchestrated generalized seizure

Epidemiology

Race: No racial preponderance.

Sex:  No Sex-based  differences

Age:

first 4 weeks of life in a full-term infant -44 weeks from conception for premature infants.

most frequent during the first 10 days of life.

Classification

  1. Clinical Seizure
  • Subtle
  • Tonic
  • Clonic
  • Myoclonic

Classification

  1. Electroencephalographic seizure
  • Epileptic
  • Non-epileptic

Clinical Classification

1.Subtle

Most common subtype

  • More in preterm than in term
  • Eye deviation (term)
  • Blinking, fixed stare (preterm)
  • Repetitive mouth and tongue movements
  • Apnea
  • Pedaling and tonic posturing of limbs

Clinical Classification

  1. Tonic
  • Primarily in Preterm
  • May be focal or generalized
  • Sustained periods of muscle contraction
  • Sustained extension of the upper and

lower limbs (mimics decerebrate posturing)

  • Sustained flexion of upper with extension of

lower limbs (mimics decorticate posturing)

  • Signals severe ICH in preterm infants
  • Generally poor prognosis

Clinical Classification

  1. Clonic
  • Primarily in term
  • Focal or multifocal
  • Biphasic –Fast contraction, Slow relaxation
  • Clonic limb movements(synchronous or

asynchronous, localized or often with no anatomic order of progression)

  • Consciousness may be preserved
  • Signals focal cerebral injury

 

Clinical Classification

  1. Myoclonic
  • Rare
  • Focal, multifocal or generalized
  • Lightning fast contractions-like jerks of extremities

(upper > lower)

Signify diffuse –serious brain injury

Electroencephalographic seizure

  1. Epileptic
  • Consistently associated with electro-cortical seizure activity on the EEG
  • Cannot be provoked by tactile stimulation
  • Cannot be suppressed by restraint of involved limb or repositioning of the infant
  • Related to hyper synchronous discharges of a critical mass of neuron

Electroencephalographic seizures

  1. Non-epileptic
  • No electro-cortical signature
  • Provoked by stimulation
  • Suppressed by restraint or repositioning
  • Brainstem release phenomena (reflex)

SEIZURE MIMICS

Jitteriness

Apnoea

Benign neonatal sleep myoclonus

APNOEA

Epileptic

Lasts <10-20 sec

Tachycardia

monorrhythmic

Nonepileptic

>10-20 sec

Bradycardia

No EEG signs

Benign neonatal sleep myoclonus

Nonepileptic form of myoclonus

1 wk of life

Resolves spont. Over weeks or months

A/E- Transient dysmaturity of brainstem reticular activating system

Movement abolished by arousal

Never occur  in awake state

No EEG findings

Etiology

  • It is critical to recognize neonatal seizures, to determine their etiology, and to treat them for three major reasons:
  1. Seizures are usually related to significant illness, sometimes requiring specific therapy

Etiology

2.Neonatal seizures may interfere with important supportive measures, such as alimentation and assisted respirations for associated disorders.

3.Experimental data give some reason for concern that under certain circumstances the seizure per se may be a cause of brain injury.

Etiology

  • Clinical history provides important clue
  • Family history may suggest genetic syndrome
  • Many of these syndromes are benign
  • In the absence of other etiologies, family history of seizures may suggest good prognosis

 

Etiology

  • Pregnancy history is important
  • Search for history that supports TORCH infections
  • History of fetal distress, preeclampsia or maternal infections

Etiology

  • Delivery history
  • Type of delivery and antecedent events
  • Apgar scores offer some guidance
  • Low Apgar score without the need for resuscitation and subsequent neonatal intensive care is unlikely to be associated with neonatal seizures

Etiology

  • Postnatal history
  • Neonatal seizures in infants without uneventful antenatal history and delivery may result from postnatal cause
  • Tremulousness may be secondary to drug withdrawal or hypocalcemia
  • Temperature and blood pressure instability may suggest infection

First 24 hours

Hours: 24 to 72

72 hours to 1 week

Benign familial neonatal seizures

Autosomal dominant

No obivious risk factors

2nd or 3rd day of life, recur for days or weeks

Ictal EEG : sudden brief period of generalized voltage attenuation

C/F: apnoea, tachycardia and tonic posturing

No antiepileptic treatment required

Benign idiopathic neonatal seizures

Normal neonatal course

Birth after 39 weeks

Seizure on day 4 to 6

Normal neurological state

clonic posturing

Normal EEG

Laboratory Studies to Evaluate Neonatal Seizures

Indicated

Complete blood count, differential, platelet count; urinalysis

Blood glucose (Dextrostix), BUN, Ca, P, Mg, electrolytes

Blood oxygen and acid-base analysis

Blood, CSF and other bacterial cultures

CSF analysis

EEG

EEG

EEG  seizure-repetitive series of electrical discharges  that evolves in frequency, amplitude

Normal rhythmic EEG pattern  –Age specific

EEG seizure is less common before 34 weeks

Frequency increases with increasing maturity

Unlike older children neonatal interictal

EEG can’t predict risk of future seizures

Laboratory Studies to Evaluate Neonatal Seizures

Clinical Suspicion of Specific Disease

Serum immunoglobulins, TORCH antibody titers, and viral cultures

Blood and urine metabolic studies (bilirubin,ammonia, lactate, FECl³, reducing substance.)

Blood and urine toxic screen

Blood and urine amino and organic acid screen

CT or ultrasound scan

Treatment

  • Identify the underlying cause:

hypoglycemia – D10 solution

hypocalcemia –  Calcium gluconate

hypomagnesemia- Magnesium sulfate

pyridoxine deficiency- Pyridoxine

meningitis- initiation of antibiotics

Treatment

  • To minimize brain damage
  • Some controversy when to start

     Anticonvulsants

  • If seizure is prolonged (longer than 3  minutes), frequent or associated  with cardiorespiratory disturbance

Acute therapy of neonatal seizures

  • If with hypoglycemia- Glucose 10%: 2ml/k IV
  • If no hypoglycemia- Phenobarbital:20mg/k IV

loading dose  If necessary : additional phenobarbital:  5 mg/kg IV to a max of 20 mg/kg

(consider omission of this additional  Phenobarbital  if with baby is asphyxiated)

Phenytoin: 20 mg/kg, IV (1 mg/kg/min)

Lorazepam:0.05-0.10 mg/kg, IV

 

Determinants of Duration of anticonvulsant therapy for neonatal seizures

  • Neonatal neurological examination
  • Cause of neonatal seizure
  • Electroencephalogram

WHEN TO DO EEG?

As soon as a seizure occurs

Within 24 hours

Continuous EEG monitoring

Interictal EEG normal –nonepileptic process

EEG abnormal-video EEG monitoring

Repeat EEG at 1 wk duration

Duration of anticonvulsant therapy-Guidelines

Neonatal period

  • If neonatal neurological examination becomes normal discontinue therapy
  • If neonatal neurological examination is persistently abnormal,consider etiology and obtain EEG
  • In most such cases- Continue phenobarbital

– Discontinue phenytoin

– Reevaluate in 1 month

Duration of anticonvulsant therapy-Guidelines

One month after discharge

  • If neurological examination has become normal, discontinue phenobarbital
  • If neurological examination is persistently abnormal,obtain EEG
  • If no seizure activity on EEG, discontinue phenobarbital

Prognosis

Two  most useful approaches in utilizing outcome

 

  • EEG
  • Recognition of the underlying neurological disease

Prognosis of Neonatal seizures in relation to EEG

EEG NEURO.SEQUELE

BACKGROUND              

Normal                10

Severe abnormalities  90

Moderate abnormalities     50 

  

Cause  Development 

Hypoxic-ischemic encephalopathy

Intraventricular hemorrhage

Subarachnoid hemorrhage

Hypocalcemia

Early-onset

Later-onset

Hypoglycemia

Bacterial meningitis

Developmental malformations

Benign familial neonatal convulsions

Complications

  • Cerebral palsy
  • Hydrocephalus
  • Epilepsy
  • Spasticity
  • Feeding difficulties

Consultations

  • Neurology consult needed for

– evaluation of seizures

– evaluation of EEG and video EEG

     Monitoring

– management of anticonvulsant

medications

Further Outpatient Care

  • Developmental evaluation for early identification of physical or cognitive deficits
  • Orthopedic evaluations if with joint deformities
  • Consider physical medicine/physical therapy referral if indicated